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From Karolinska Institutet Department of Clinical Sciences

Psychiatry Section Danderyd University Hospital

Stockholm, Sweden

Mild traumatic brain injury –

clinical course and prognostic factors for postconcussional disorder

Anders Lundin

Stockholm 2007

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Cover image: Mohawk. Detail from a terracotta sculpture by Magnus Ringborg. Photo by Magnus Ringborg (www.magnusringborg.se) Graphic design: Henrik Löfgren

All published papers reproduced with the kind permission of the publishers Printed by Universitetsservice US-AB

Nanna Svartz väg 4, SE-171 77 Stockholm, Sweden

© Anders Lundin, 2007 ISBN 91-7357-078-8

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“The late effects of head injury can only be properly understood in the light of a full psychiatric study of the individual patient. It is not only the kind of injury that matters, but the kind of head that is injured that determines recovery of function”

Sir Charles Symonds (1937), British neurologist, in Mental disorder following head injury; Proceedings of the Royal Society of Medicine.

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Abstract

Background

Mild traumatic brain injury (MTBI) is frequent and sometimes leads to persistent disability. It remains a matter of controversy as to what impact the different main determinants – brain injury factors and psychosocial fac- tors – exert on the development of postconcussional disorder (PCD).

Aims, subjects and methods

The overall aim was to find predictors for PCD after MTBI. One hundred and twenty-two persons with MTBI were assessed with CT and MRI brain scans, S 100B, S 100A1B, and clinical variables. The first week after the trau- ma an extended assessment was performed, including previous history of psychiatric disorder, psychological function the year before the trauma, per- sonality, coping ability, and concurrent psychosocial stressors. Three months post injury outcome was assessed by use of established self assessment ques- tionnaires for MTBI related symptoms and disability. Cognitive impairment was assessed with a computerized Automated Psychology Test (APT) and neuropsychological testing. Thirtyfive healthy control persons were assessed for comparison.

Results

Is increased S 100 associated with cognitive impairment?

S 100B and S 100A1B were increased in 42 % and 64 % of the patients and in 60 % and 80 % of those with radiological signs of hemorrhage, respec- tively. Cognitive impairment was found in 8 % when assessed with APT and in 30 % when assessed with neuropsychological tests. No significant correla- tion was found between S 100B or S 100A1B and cognitive impairment, nor between subjectively reported cognitive dysfunction and test performance, regardless of the method used.

What is the clinical course after MTBI?

At least one persisting symptom was reported by 49 % of the patients at three months – most commonly poor memory, sleeping problems and fatigue. High symptom load at day one correlated with high symptom load and disability at three months, when 25 % also reported disability in at least one domain of everyday life.

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How should PCD be defined?

The ICD-10 definition of PCD was considered too liberal as no disability was required. The results from neuropsychological testing had insufficient specificity to qualify, as proposed in the DSM-IV, as a defining property of PCD. A definition of PCD based on a minimum of three symtpoms and two domains of disability at three months post injury was proposed, which yielded 17 % PCD cases in the whole sample.

Which risk factors predict the development of PCD?

Preinjury psychological vulnerability (previous psychiatric disorder, trait anxiety, embitterment), lower preinjury psychological function (GAF) and concurrent psychosocial stressors were significant predictors of PCD.

Posttraumatic stress (hyperarousal) one week after the MTBI had the high- est impact on the outcome. Female gender and concurrent medical condi- tion were also correlated to PCD, but no correlation was found between PCD and injury related factors.

In summary, signs of brain injury or brain dysfunction are present in the early phase after MTBI but show poor correlation to PCD as defined by at least three symtpoms in combination with disability at three months post injury. The results from neuropsychological testing had insufficient speci- ficity to qualify as a defining property of PCD. Prognosis after MTBI is good in most cases, but a minority of patients develop PCD, which emerges as a result of the interaction between premorbid psychological vulnerability, brain dysfunction in the early phase, posttraumatic hyperarousal and con- current psychosocial stressors.

Keywords: Mild traumatic brain injury, S 100, cognitive impairment, symp- toms and disability, postconcussional disorder, prognostic factors

ISBN 91-7357-078-8

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List of publications

I S 100 and cognitive impairment after mild traumatic brain injury.

Catharina de Boussard, Anders Lundin, Daniel Karlstedt, Gunnar Edman, Aniko Bartfai, Jörgen Borg.

Journal of Rehabilitation Medicine 2005; 37: 53–57 II Symptoms and disability until 3 months after mild TBI.

Anders Lundin, Catharina de Boussard, Gunnar Edman, Jörgen Borg.

Brain Injury, July 2006; 20(8): 799–806

III A comparison of three criteria sets for postconcussional disorder after mild traumatic brain injury.

Anders Lundin, Catharina de Boussard, Daniel Karlstedt, Aniko Bartfai, Gunnar Edman, Jörgen Borg.

(submitted)

IV Prognostic factors for postconcussional disorder after mild traumatic brain injury.

Anders Lundin, Catharina de Boussard, Gunnar Edman, Jörgen Borg.

(submitted)

Study I and II reprinted with kind permission of the Taylor & Francis Group.

Study IV reprinted with kind permission of the British Journal of Psychiatry.

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List of abbreviations

APT Automated Psychological Test system AUDIT Alcohol Use Disorders Identification Test BBB Blood Brain Barrier

CI Confidence Interval

CT Computerized Tomography (of the brain)

DSM-IIIR Diagnostic and Statistical Manual of mental disorders, third edition, revised

DSM-IV Diagnostic and Statistical Manual of mental disorders, fourth edition

ED Emergency Department

ELISA Enzyme Linked ImmunoSorbent Assay GAF Global Assessment of Function

GCS Glasgow Coma Scale

HADS Hospital Anxiety and Depression Scale

ICD-10 International Classification of Diseases, tenth revision ICF International Classification of Functioning, Disability and

Health

IES-R Impact of Event Scale – Revised KSP Karolinska Scales of Personality LOC Loss Of Consciousness

MRI Magnetic Resonance Imaging (of the brain) MTBI Mild Traumatic Brain Injury

OR Odds Ratio

PCD PostConcussional Disorder*

PCS PostConcussional Syndrome*

PTA PostTraumatic Amnesia

PTSD PostTraumatic Stress Disorder

RHFUQ Rivermead Head injury Follow Up Questionnaire RPQ Rivermead Post Concussion Symptoms Questionnaire S 100 Soluble in 100 % ammonium sulfate saturated solution SOC Sence Of Coherence scale

SSP Swedish universities Scales of Personality TBI Traumatic Brain Injury

* In previous studies, the terms PCD and PCS are often used interchangeably. In Paper III the appropriateness of the two terms is discussed.

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Contents

Background 13

Assessments of brain injury 14

Clinical course and outcomes in previous studies 18

The controversy 25

The biopsychosocial model 25

Aims 29

Subjects and methods 31

Inclusion and exclusion criteria 31

Study setting and study sample 31

Patients 32

Withdrawal during study 32

Controls 32

Procedure 32

Assessments 34

Statistical methods 41

Results 43

Sociodemographic and clinical characteristics 43

Paper I–IV 43

Summary of results 56

Discussion 57

Methodological issues 57

Paper I–IV 63

Summary of findings 75

Conclusions and future research 77

Populärvetenskaplig sammanfattning på svenska 79

Acknowledgements 83

References 85

Appendix 96

Rivermead Post Concussion Symptoms Questionnaire (in Swedish) 96 Rivermead Head Injury Follow Up Questionnaire (in Swedish) 97 Paper I–IV

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Background

Traumatic brain injury (TBI) is a common event in the population. Mild traumatic brain injury (MTBI) represents between 70 - 90 % of all TBI cases that present at hospitals, and the incidence of hospitalized adults with MTBI is about 200/100.000 in Sweden [1]. Falls are the most common cause and motor vehicle and bicycle injuries are the second and third most com- mon causes of MTBI. Many individuals with MTBI do not seek medical help and the actual rate of MTBI, based on several population studies, is calculated to be over 600/100.00 per year [2]. The risk is greatest among young male adults – the male/female ratio is about 1.5/1.

There has been some controversy as how to define MTBI, and in previous research different definitions have been used, leading to some confusion.

The American Congress of Rehabilitation Medicine in 1993 has therefore agreed on the following defintion:

A patient with MTBI is a person who has had a traumatically induced physiological disruption of brain function as manifested by at least one of the following:

any period of loss of consciousness;

any loss of memory for events immediately before or after the accident;

any alteration in mental state at the time of the accident (e.g., feeling dazed, disoriented, or confused); and

focal neurological deficit(s) that may or may not be transient but where the severity of the injury does not exceed the following:

loss of consciousness of approximately 30 minutes or less;

after 30 minutes, an initial Glasgow Coma Scale (GCS) of 13-15;

post traumatic amnesia (PTA) not greater than 24 hours.

There are several ways – clinical, radiological and biochemical – of establish- ing the severity and immediate consequenses of the brain injury after a concussion. This is of importance for the acute management of the patients after presenting at the emergency ward. The acute indices of severity also constitute the basis for prognosis.

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Assessments of brain injury

Clinical assessment

The duration of amnesia after MTBI, posttraumatic amnesia (PTA), is used as one of the defining criterias (< 24 hours), but there are few studies to support the reliability of this symptom. PTA is also referred to as anterograde amnesia, meaning inability to recall events immediately following the trauma.

The PTA ceases when the individual is able to report coherent memories from the period after the trauma. PTA should ideally be established prospectively at the ED but crucial additional information can sometimes be obtained retrospectively through a thorough analysis of the patient´s history.

The duration of loss of consciousness (LOC) is another defining criterion (< 30 minutes) for MTBI. The clinically most elaborated and frequently used method to assess the level of consciousness is the Glasgow Coma Scale (GCS) score, see table 1.

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Score Motor response Eye opening Verbal response

1 None None None

2 Extension to pain Opens to pain Incomprehensible 3 Flexion to pain Opens to command Inappropriate words 4 Withdrawal from pain Opens spontaneously Confused, disoriented

5 Localising pain - Normal

6 Obeys commands - -

y

GCS score Severity of brain injury 3 – 8 Severe

9 – 12 Moderate 13 – 15 Mild

Table 1. Glasgow Coma Scale

Table 2. GCS score and TBI severity

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Assessment of GCS when the patient presents at the ED is the gold standard for grading of the severity of TBI, see table 2, and has been used as a guide for the acute management as well as for prognostic purposes.

A GCS score of 13 – 15 is thus consistent with “mild” traumatic brain injury. It has been proposed, though, that patients presenting with a GCS score of 13 should be classified as “moderate”, as their prognosis in terms of acute complications and intracranial lesions are similar as for those patients who are moderately injured [3, 4]. Other symptoms and signs of clinical importance in the acute phase are vomiting, seizures and retrograde amnesia, i.e. inability to recall events that occurred before the trauma.

Brain imaging

Skull X-rays is sensitive for detecting skull fractures, which is a risk factor for intracranial complications, but the diagnostic accuracy with regard to these complications is poor [5]. The method has become of less importance since the introduction of the more sensitive computed tomography brain scan (CT) and magnetic resonance imaging of the brain (MRI). A Canadian study of 3121 patients with MTBI showed clinically important intracranial lesions in 4.8, 17.2 and 40.9 % of the patients with a GCS score of 15, 14 and 13 respectively [6]. MRI is more sensitive than CT to detect intracranial pathology [7].

With recent improvements, such as diffusion-weigthed MRI and diffusion tensor imaging, the MRI techniques have become even more sensitive than standard MRI [8] and have shown that diffuse axonal injury occurs more often than previously assumed [9]. Proton magnetic resonance spectroscopy studies have also indicated presence of cellular injury in frontal white matter that on conventional MRI appeared normal after MTBI [10]. Functional MRI, used in small studies to objectify brain injury after con-cussion, have shown different patterns of activation in concussed patients as compared to controls, even in the absence of observed deficits in behavioral performance [11]. Some studies indicate that flow deficits observed with SPECT better reflect the magnitude of the brain damage than CT [12], and PET has been used to visualize frontotemporal hypometabolism in MTBI patients with persistent cognitive impairment [13]. However, these techiques are not yet established tools for routine assessment of patients with concussion.

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Biochemical markers

Damage to neurons and neuronal supporting cells causes release of proteins, some of which enter the cerebrospinal fluid, cross the blood-brain barrier (BBB) and leak into the peripheral circulation, where they can be measured by use of blood samples. Neuron-specific enolase and cleaved-tau are con- sidered markers for neuronal damage [14, 15], whereas damage to supporting cells such as astrocytes and oligodendrocytes is reflected in increased serum levels of S 100B, creatine kinase BB isoenzyme and myelin basic protein [16- 18]. Several factors, such as intrathecal concentration, metabolic consump- tion or reuptake, BBB disruption, molecular size, half-life, sensitivity and specificity of the assay and contamination of the marker from other sources in the body possibly affect the serum concentration of these markers and confound the interpretation of the measurements.

Most studies concerning biomedical markers have been performed on S 100B, a polypeptide belonging to a larger family of calciumbinding proteins, called S 100 due to its solubility in 100 % Saturated ammonium sulphate.

S 100B has both intracellular and extracellular functions and exerts, depend- ing on its concentration, neurotrophic as well as toxic effects [19]. S 100B is correlated to outcome in neurological disorders like stroke and global hypoxia. In severe brain injury a significant relation between outcome and initial S 100B concentration in blood has been shown [20]. However, short half-life (97 minutes), lack of specificity for neural tissue – S 100 is also found in fat and muscle cells outside the brain, and increased levels have been observed after bone fractures and contusions [21] – and uncertainty whether S 100B reflects parenchymal damage or BBB dysfunction are con- founders that have resulted in conflicting evidence as to the clinical utility of this marker for diagnostic and prognostic purposes in MTBI patients [20].

In a previous paper from our cohort of patients with MTBI [22] it was demonstrated that serum concentrations of S 100B were significantly higher in MTBI patients (z=3.94, p<0.001) as well as in patients with mild orthopaedic injuries (z=3.99, p<0.001) as compared to non-injured persons.

S 100B and S 100A1B concentrations in MTBI patients were initially increased, as well as the number of patients with values above cut off limits, and decreased rapidly over time, see figures I and II. Initial S 100B concen- trations were higher in MTBI patients with CT and/or MRI abnormalities (60 % above cut off) than those without CT and/or MRI abnormalities (38

% above cut off). There was no correlation between concentrations of S 100

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and symptom reports at three months. In summary, the diagnostic accuracy of S 100B and S 100A1B for MTBI was poor. Serum concentrations were not correlated to the severity of injury nor to symptom reports at three months post injury.

S100B

0,000 0,020 0,040 0,060 0,080 0,100 0,120 0,140 0,160

Acute Day 1 Day 14

Time

Concentrationug/L

0%

10%

20%

30%

40%

50%

60%

70%

Percentageofpatietnswithconcentrationsabovecutoff

Bars: mean values of S100B

Line: percentage of patients with S100B concentrations above cut-off

S100A1B

0,000 0,020 0,040 0,060 0,080 0,100 0,120 0,140 0,160

Acute Day 1 Day 14

Time

Concentrationug/L

0%

10%

20%

30%

40%

50%

60%

70%

Percentageofpatientswithconcentrationsabovecutoff

Bars: mean values of S100A1B

Line: percentage of patients with S100A1B concentrations above cut- off

Figure 1. Time course of S100B in patients with MTBI

Figure 2. Time course of S100A1B in patients with MTBI

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An association between the APOE epsilon4 allele and decreased cognitive performance after mild head injury has been found. In a population-based longitudinal study, within-person comparisons of probands exposed to mild head injury with the epsilon4 allele showed decreased cognitive performance, whereas injured probands without the allele were unchanged [23]. The prospective design of the study yields ideal conditions for comparing prein- jury with postinjury performance at the individual level. Later prospective studies have not been able, though, to replicate the finding when comparing, at group level, neuropsychological outcome after MTBI in persons with and without the allele[24].

In summary, there is converging evidence that MTBI is associated with various signs of organic brain injury or dysfunction, although the long term prognostic significance of these findings for the development of persistant disability remains unclear.

Clinical course and outcome in previous studies

Heterogeneity in previous studies

Different observation periods, such as 6 weeks [25], 3 months [26-29] and one year [30, 31] have been used.

Case definitions range from at least one reported symptom [25, 26, 29, 30], significant ongoing problems [28] to at least three symptoms [32].

Control groups have included for example patients exposed to an orthopedic trauma [28], patients from different medical settings [33], uninjured subjects and their relatives [34], patients with traumatic back pain [35] and a matched control group [27]. Several authors have shown no or only minor significant differences in symptoms between exposed and non exposed individuals [34, 35], whereas others have reported some significant differ- ences in endorsement of a limited number of symptoms (doing things slowly, fatigue and poor balance), especially when frequency as well as severity of symptoms have been measured [36].

Symptoms and disability

Most prominent symptoms at follow up have been headache, irritability and dizziness [25], headache, dizziness, fatigue and difficulty in concentration [26], headache and concentration difficulties [28], headache and dizziness [29], concentration problems and restlessness [34], headache, decreased

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energy and dizziness [27]. Lack of consistency of the different symptoms have been pointed out by several authors [25, 26].

In a prospective study by Lidvall et al on 83 patients headache was the most commonly reported symptom (58 %), followed by dizziness, fatigue and difficulty in concentration [26]. Three months after the trauma 24 % of patients reported at least one symptom, attributed to the accident. In the early phase after the accident headache and dizziness dominated. Later the picture became more polymorphous. One out of three patients reported new symptoms, anxiety (anxiousness, nervousness, restlessness, mental tension) being the most common of these, followed by fatigue.

In a study by Ponsford et al of 84 MTBI patients, frequency and intensity of MTBI symptoms were measured one week and three months after injury and compared to controls, exposed to an orthopedic trauma [28]. One week after the trauma, MTBI patients showed significantly more symptoms than controls, specially headache, dizziness, irritability, fatigue and sleeping diffi- culty. Three months after injury, however, only the intensity of headache and concentration difficulties were greater in patients than in controls.

Neuropsychological testing at three months showed no differences between patients and controls.

In a study by Bohnen et al of 71 MTBI patients, a principal component analysis of the post-concussive symptoms resulted in a two factor solution [37]. One factor (post-concussive-cognitive complaints) consisted of ”typical post-concussional symptoms” such as headache, dizziness, intolerance to light, noise and other external stimuli together with items indicating problems with decreased work capacity and efficiency, tiredness, difficulty doing things simultaneously, and diminished concentration. The other factor (emotional-vegetative) included complaints of heart palpitations, wet hands, dyspnoe, flushing, problems with digestion, having a tense feeling in the chest as well as items of depression, emotional lability, restlessness and decreased libido. Patients with lasting symptoms had either a history of previous MTBI or preexisting emotional distress.

In a three-center study of neurobehavioural outcome in patients admitted to hospital after minor head injury, Levin et al assessed 57 patients within 1 week (baseline) after head injury and at 1 and 3 months postinjury [27]. A matched control group was used and patients with a history of previous

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head trauma or neuropsychiatric disorder were excluded. Cognitive impair- ments demonstrated at baseline resolved during the first three months after the injury. Subacute postconcussion symptoms reported were headache in 71 %, decreased energy in 60 % and dizziness in 53 % of the cases. The incidence of symptoms at three months was: 47 % for headache, 22 % for decreased energy and 22 % for dizziness. Symptoms were grouped into three domains: somatic, cognitive and affective.

In a study by Middelboe et al, 28 patients admitted for neurological care were followed for one year after mild head injury [30]. Patients with previous neurologic or psychiatric disorder were excluded from follow up. At one year headache was reported by 32 %, dizzines, memory deficit and concen- tration deficit by 25 % and fatigue and irritability by 21 % of the patients.

According to the definition of postconcussional syndrome (PCS) in this study – one or more symptoms attributed to MHI and/or occurence of significantly elevated score on GHQ-60 (General health questionnaire) and IES (Impact of event scale), two self-report measures of general wellbeing and level of posttraumatic stress, respectively – 50 % of the patients were cases at one year follow up.

Specificity of symptoms

In a small study by Gasquoine, symptom change reports in patients with concussion were compared with patients with traumatic back pain [35].

Even when only selected local head and cognitive dysfunction postconcus- sional symptoms were analyzed, there was no difference between the two groups, indicating a lack of specificity for the postconcussion symptoms.

In a study by Fox et al, base rates of postconcussive symptoms were deter- mined in patients from different medical settings and controls and compared to patients with a recent history (within two years) of being knocked unconscious or bumping the head without losing consciousness [33].

Patients having been knocked unconscious or with a bump on the head reported more symptoms than those without head injury, but neurological, psychological and environmental variables – without any associated head injury – were also significantly related to PCS complaints. The knocked unconscious group reported a headache rate of 52 % and a fatigue rate of 60 % – symptoms normally considered core symptoms of PCS – which did not differ significantly from the unknocked group. The study points to the importance of disentangling the change in symptom perception post injury 20

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as compared to symptoms at baseline. The study also indicated that the severity of symptoms, i e not only the frequence, in concussed patients compared to controls has to be assessed.

In summary, a variety of symptoms and behavioural changes are common in the acute stage after MTBI but a majority of patients recover within 3 – 12 months. Many methods have been used to evaluate outcome, but hetero- geneity of study samples, study designs, follow-up periods and selection of outcome criteria have made comparisons between studies difficult and have complicated the interpretation of data [38]. The most commonly used outcome domains are cognitive function, persisting subjective symptoms and disability or need for surgical intervention and mortality. Unfavourable recovery after concussion is often referred to as Postconcussional syndrome (PCS) or Postconcussional Disorder (PCD). However, although discussed during more than a century, an unequivocal definition of the condition is still lacking (see below).

Cognitive impairment

Cognitive impairment is one of the domains of symptoms and disability.

Subjective complaints of slowness of thought, memory problems and concentration difficulties are common after MTBI. Neuropsychological tests assess cognitive function, and several studies have been performed to evaluate the extent and type of cognitive impairment after MTBI with a variety of cognitive test batteries.

In a study by Levin et al cognitive impairment in the domains of memory, attention, and information-processing speed was present the first month after MTBI but was generally resolved after three months [27]. Subjective complaints tended to persist in cases even after recovery of cognitive function.

In a study by Hugenholtz, MTBI patients were significantly slower than the normal control group on the choice reaction time tests, which demanded an increased amount of attention and information processing during the 1st month after injury. The performance improved gradually, but minor differences were still present after three months [39].

In a study by Bohnen et al, MTBI patients with postconcussional symptoms six months post injury showed deficits in selective and divided attention as compared to patients without symptoms [40].

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In a study by Killam et al, in which non-concussed, non-recent-concussed and recent-concussed athletes were compared, the findings indicated that recent head injury resulted in demonstrable memory problems, that resolved with time. There was an inverse correlation between the severity of the postconcussion score and scores for attention and delayed memory [41].

In summary, cognitive impairment is demonstrated for attention, memory and speed of processing after MTBI, but in most studies problems resolve with time and residual impairment are in most studies insignificant or difficult to demonstrate when MTBI patients are compared with control groups. More- over, in some studies there is poor correlation between neuropsychological test results and the subjective reporting of symptoms.

Postconcussional syndrome / Postconcussional disorder The concept of PCS, “postconcussional syndrome”, has been criticised. The label of a “syndrome” would ideally require a more consistent association between the described symptoms and the supposed underlying patho- physiological mechanism. Moreover, the failure to identify any clear “point of rarity” for the condition, the lack of an association with a condition specific biological marker and the absence of effective, validated treatments do not support the existence of a discrete disease entity.

The multisymptomatic condition has phenomenological overlaps to multi- symptomatic functional illnesses such as chronic pain and chronic fatigue [42], and the mix of somatic and psychological complaints is also found in several psychiatric disorders, such as depression, posttraumatic stress disorder (PTSD) and generalized anxiety disorder. The prevalence of depressive disorder after MTBI is about 20 - 25 % [43, 44], and 33 % after TBI [45].

PTSD have been found in 48 % of patients three months after having been knocked unconscious in a traffic accident and in 33 % after one year [46].

Thus, there is a basis for conflicting views as to whether PCS is in fact caused by the concussion or if it is just an alternative conceptualization of the emotional, cognitive and somatic symptoms that do also occur in functional somatic syndromes or depressive and anxiety disorders, or wheter the intensity of the symptoms of brain injury are just fueled by comorbid depression or PTSD. Although attribution of the symptoms to effects of the head injury seems logical and straightforward, the association is not uncomplicated. There are diverging opinions within the medical soci- ety about the nature of the illness as well as what determinants should be 22

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considered crucial. For example, in a recent systematic review of MTBI the view was taken that the current labels in use for the condition – postconcussion syndrome and postconcussional disorder – were potentially misleading because of the implication that the symptoms de facto are a result of the concussion [38], a phenomenon elsewhere referred to as the “reification fallacy” [47].

The two existing formal definitions of PCS and PCD according to ICD-10 and DSM-IV are rarely used in MTBI studies. The DSM-IV diagnosis is just a proposed criteria set for further study and not an established new category.

The ICD-10 formulation has been subject to substantial criticism. The pres- ence of postconcussion-like symptoms are not unique to mild head injury.

The symptoms are commonly found in healthy individuals and are highly correlated with depressive symptoms [48]. In one recent study, the ICD-10 PCS symptoms were unable to accurately classify the MTBI patients at three months post-injury [49]. Moreover, the ICD-10 and the DSM-IV defini- tions exhibit important differences [50-53], see table 3.

In addition to the head injury criterion, the DSM-IV definition requires disability and cognitive deficits verified by neuropsychological testing, wheras the two ICD-10 definitions only require presence of at least three symptoms for a diagnosis of PCS. Furthermore, the DSM-IV definition comprises changes in personality and apathy/lack of spontaneity as symptoms, thus bringing the definition of PCD closer to the concept of brain damage in the more severe end of the spectrum. The ICD-10 definition on the other hand includes “preoccupation with the symptoms and fear of permanent brain damage to the extent of hypochondriacal concern, over- valued ideas and adoption of sick role”. The ICD-10 definition thus concept- ualizes the illness in a more psychological way, whereas the DSM-IV definition puts the symptoms in a biomedical frame of reference, requiring “evidence from neuropsychological testing” of cognitive difficulties in addition to sub- jectively experienced and expressed symptoms. The differences are also seen in the DSM-IV definition of “significant concussion”, which requires two of the following criteria: 1. a period of unconsciousness lasting more than 5 minutes, 2. a period of posttraumatic amnesia that lasts more than 12 hours after the closed head injury, or 3. a new onset of seizures that occurs within the first 6 months after the injury, whereas ICD-10 requires only the more unspecific “history of head trauma with loss of consciousness”.

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p ICD10 (1992clinicalguidelines)ICD10 (1993researchcriterias)DSM-IV (1994proposedcriteria) Symptoms(S-criterion) Followingsymptomsoccurinall threedefinitions: -headache -dizziness -fatigue -irritability -emotionallability -insomnia SymptomsintheICD10definitions thatdonotoccurintheDSM-IV: -subjectivecognitivecomplaints SymptomsintheDSM-IVthatdo notoccurintheICD10definitions: -changesinpersonality -apathyorlackofspontaneity Atleastthreeofthefollowing features 1.headache 2.dizziness 3.fatigue 4.irritability 5.difficultyinconcentratingand performingmentaltasks 6.impairmentofmemory 7.insomnia 8.reducedtolerancetostress, emotionalexcitementand alcohol 9.depression/anxiety 10.fearofpermanentbrain damage 11.hypochondriacalconcerns 12.adoptionofasickrole Atleastthreeofthefollowingfeatures 1.somaticsymptoms(headache,dizziness, malaise,fatigue,noiseintolerance) 2.affectivesymptoms(irritability, emotionallability,depressionand/or anxiety) 3.cognitivesymptoms(subjective complaintsofdifficultyinconcentration,in performingmentaltasksandmemory complaints,withoutclearobjective evidenceofmarkedimpairment) 4.insomnia 5.reducedtolerancetoalcohol 6.preoccupationwiththeabovesymptoms andfearofpermanentbraindamagetothe extentofhypochondriacalconcern, overvaluedideasandadoptionofsickrole.

Atleastthreeofthefollowingfeatures 1.becomingfatiguedeasily 2.disorderedsleep 3.headache 4.vertigoordizziness 5.irritabilityoraggression 6.anxiety,depressionoraffectivelability 7.changesinpersonality 8.apathyorlackofspontaneity Disability(D-criterion)NotrequiredNotrequiredSignificantimpairmentinsocialor occupationalfunctioning Objectivesignsofcognitive dysfunction(NP-criterion)NotrequiredNotrequiredEvidencefromneuropsychologicaltesting ofdifficultyinattention(concentrating, shiftingfocusofattention,performing simultaneouscognitivetasks)ormemory (learningorrecallinginformation)

Table3.Criteriaforpostconcussionalsyndrome/disorderaccordingtotheclassificationsinICD-10andDSM-IV. Traumaandexclusioncriteriaarenotpresented.

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The controversy

The determinants of the clinical course after MTBI have been a matter of controversy for more than 100 years. The traditional biomedical model, emphasizes cerebral dysfunction factors, and presupposes that symptoms and disability result from and could be understood as consequences of the cerebral damage caused by the trauma. This way of understanding the suffering and the disability also seems to be the most common way to inter- pret the problems among lay people. However, several studies of the conse- quenses of MTBI have failed to show such a straightforward correlation between injury and outcome, as mild injuries with a similar acute impact can lead to grossly divergent outcomes. Instead, an increasing amount of studies have demonstrated impact from non-injury, contextual and personal factors, and the long term disabilities after an MTBI have in most cases remained unaccounted for by demonstrable anatomical and physiological changes.

The biopsychosocial model

The International Classification of Functioning, Disability and Health (ICF), was published in 2001 on behalf of World Health Organization (WHO) [54]. Body structure/body function, activity and participation are main components in this model, and these interact both with each other and with contextual and personal factors at different levels.

The ICF applies a biopsychosocial perspective to obtain a synthesis of the medical and the social model of understanding disability. A biopsychosocial model of understanding is often applied for the understanding of subjective health complaints that are not fully accounted for by demonstrable patho- logic changes. In several common disorders no objective signs of physical pathology can be demonstrated. In primary care about one third of somatic symptoms lack medical explanation [55]. Medically unexplained symptoms are often chronic and strongly associated with depressive and anxiety disorders.

The biopsychosocial model was first formulated by psychiatrist George Engel [56]. Engel acknowledged the advances of biomedical research but problematized its omniscient claims. In the biopsychosocial model, illness is viewed as the result of interaction of a multitude of causal factors, operating at different levels in different phases of the illness process. Factors that do not easily fit into the biomedical model are, for example, psychological vul- nerability, general distress, adaption of a sick role and the impact of the

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Trauma

Perpetuating factors MTBI

Pre- traumatic

factors

Outcome (PCD)

Predisposing factors

Precipitating factors

Perpetuating factors Biological Genetic factors

5-HTT, short allele ApoE, epsilon 4 allele Medical condition Sex

Age

Head injury GCS LOC PTA S 100

Inactivity Sleep disorder Drug or alcohol misuse

Psychological Premorbid personality Negative affectivity Cognitive abilities Psychological vulnerability

Prior psychiatric disorder Heredity for pscyh disorder Childhood experiences Illness experiences

Peritraumatic stress Hyperarousal Intrusions

Hyperarousal Anxiety/Depression Maladaptive coping style

Catastrophizing Avoiding Victimization Sick role adaption

Social Psychosocial stressors Financial motifs Patient support group Psychosocial stressors

Insufficient social support network Iatrogenic factors

“Diagnosis threat”

Adapted from Gallagher, R.M. (2005). “Rational integration of pharmacologic, behavioural and rehabilitation strategies in the treatment of chronic pain” Am J Phys Med Rehabil 84 (3 Suppl): S64 – 76.

Figure 3. Etiological model.

Table 4. The biopsychosocial net, adapted to possible MTBI related issues.

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patient-clinicain relationship. In the biopsychosocial model it is customary to describe the determinants of the illness process in terms of predisposing (pretraumatic), precipitating (traumatic) and perpetuating factors, as described in figure 3.

The biopsychosocial model has been summarized by Gallagher [57]. Table 4 shows the model with some adaptions of the included variables according to the MTBI research agenda.

As present MTBI research has indicated that biological as well as behavioral, psychological, social and contextual factors affect the clinical course after MTBI, a biopsychosocial model was chosen for this study as the most appropriate conceptual framework for investigating the development of PCD.

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Aims

The general aim was to contribute to the understanding of the development of PCD after MTBI.

The specific questions were:

Paper I: Is increased S 100 associated with cognitive impairment?

Paper II: What is the clinical course after MTBI?

Paper III: How should PCD be defined?

Paper IV: What are the risk factors for PCD after MTBI?

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Inclusion and exclusion criteria

Inclusion required a history of blunt head trauma, loss of consciousness (LOC) and/or posttraumatic amnesia (PTA), admission to hospital within 24 hours after the trauma, a Glasgow Coma Scale (GCS) score of 14 – 15 at first assessment in the ED and an age of 15 – 65 years. Exclusion criteria were any of the following: LOC > 30 minutes, PTA > 24 hours, other significant physical injury or other major neurological disorder, including previous significant head injury. No financial incentives were offered for participants and no specific intervention was attached to the study.

Study setting and study sample

Patients were recruited from three ED:s located in the central and north Stockholm, Sweden, between January 2000 and December 2001. The catch- ment area for the three ED:s has about 800.000 inhabitants in the age of 15 – 65 years. Mean age in the area is 38 years and about 51% are women.

Stockholm is the capital of Sweden with a high percentage of employment in white collar professions. Thirty-eight % of the population between 15 and 65 years of age have an education exceeding twelve years; the corre- sponding figure for the total Swedish population is 26 %.

Recruitment was non-systematically interrupted and covered in total 20 months at Danderyd University Hospital and 3 - 6 months in the two other hospitals (Karolinska University Hospital and Stockholm Söder Hospital).

During the recruitment periods all MTBI patients were consecutively con- sidered for inclusion. In total one hundred and twenty-two patients with MTBI fulfilled inclusion criteria and gave informed consent. The majority (75 patients) were recruited from Danderyd University Hospital, where detailed data on numbers and reasons for non-participation were collected during a three months period (from February to April 2001). During this period 27 % of the eligible patients agreed to participate. Most common reasons given for non-participation were lack of time and lack of interest and motivation for the follow up program. Age and gender did not differ between non-participants and participants. For non-participants hospital-

Subjects and methods

The study was approved by the ethics committee at the Karolinska Institutet.

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ization rate was 53 % and CT scan was performed in 60 % of the cases, none of which was abnormal. Of the participants 80 % had been hospital- ized, 93 % underwent CT scan, 7 % of which were abnormal.

Patients with high velocity traumas were managed in a tertiary trauma unit according to a regional trauma protocol and were not available for the study.

Patients

Seventy-one men (58 %) and 51 (42 %) women fulfilled the inclusion criteria and volunteered to participate in a follow up study, including six assessment sessions, a CT brain scan and an MRI brain scan. According to current rou- tines most patients (80 %) were hospitalized after admission for observation over night.

Withdrawal during study

Twenty patients (16 %) dropped out from the study during the first three months. Dropouts were compared to non-dropouts with respect to age, gender, hospital, education, occupation, PTA, LOC, initial symptom severity, previous psychiatric history and alcohol intoxication at admission. Dropouts did not differ in any variable except for significantly fewer years of education (mean difference 2.3 years).

Controls

Thirty-five subjects without history of previous head injury and in good health according to self-report and working in different professions (25 % health care workers) or studying (14 %), were recruited by means of local advertisement for assessment of base rate symptoms and neuropsychological testing.

Procedure

After information about the study, informed consent was obtained from all participating patients before inclusion in the study. GCS score, duration of LOC, PTA and retrograde amnesia and results from breath alcohol test were recorded by the ED staff according to the study protocol. The ED:s were checked for new head injury patients by the research group staff every day of the week. Included patients were assessed after 1, 7 and 14 days and at three months post-injury. CT scan of the brain was performed within 24 32

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Day 0

Day 1

Day 7

Day 14

3 mths

Patients Controls

Neuropsychology test S 100

APT RPQ GCS, LOC, PTA, ‰

S 100 CT brain scan

S 100 APT RPQ

Multiaxial assessment SSP, SOC, GAF.

HADS, IES-R, RPQ MRI brain scan

Neuropsychology test S 100

APT RPQ, RHFUQ

S 100 APT RPQ

S 100 APT RPQ S 100

APT RPQ

Procedures

hours after the trauma and an MRI scan of the brain was performed within one week (mean 7.4 days). Within one week after the injury, emergency data were reassessed with the patient and revised if additional or divergent infor- mation was reliably obtained by use of data not available at the initial assessment. At this occasion an extensive clinical investigation was also per- formed to assess pre-traumatic and post-traumatic status.

For overview and time schedule of the assessment procedures, see figure 4.

Figure 4. Assessment procedures

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Assessments

Pre-traumatic variables DSM-IV multiaxial assessment

A multiaxial assessment according to DSM-IV was performed by an experi- enced neuro-psychiatrist (AL). Previous and current psychiatric diagnosis on Axis I and Axis II according to DSM-IV criteria were established with a clinical interview. The assessment included a survey of general medical con- ditions (Axis III), and a neurological examination to detect sequelae from the recent injury and to exclude other concurrent neurological disorders.

Psychosocial and environmental problems (Axis IV) were assessed by use of the Severity of Psychosocial Stressors scale, comprising 11 “yes” or “no”

questions and the experienced level of distress was assessed on a six-graded scale (none, mild, moderate, severe, extreme, disastrous) as suggested in the DSM-III-R [58]. Comparisons between this scale and a more elaborate sys- tem for measuring life event stress (PERI), indicate that Axis IV ratings cor- relate significantly with PERI ratings of disruption associated with rated events [59]. Global Assessment of Function (GAF) was assessed by use of a self-report version of the Global Assessment of Functioning Scale according to Axis V and based on the original 0 – 100 scale [60], a valid and reliable unidimensional instrument measuring psychological, social and occupa- tional functioning [61]. GAF was assessed for the last year (“GAF-1”) and for the last two weeks (“GAF-2”) before the trauma. Family history of psy- chiatric disorder was also noted.

The patients also completed a number of self-assessment inventories:

Swedish universities Scales of Personality (SSP )

Personality traits were assessed by use of a self-rating instrument, SSP, Swedish universities Scales of Personality [62]. SSP measures personality traits of possible importance for identifying individuals at risk for psychi- atric disorders. SSP consists of 13 scales, listed and described in table 5. SSP is a revision of KSP, Karolinska Scales of Personality, a personality inventory widely used in psychiatric research [63]. KSP subscales related to anxiety proneness and hostility are associated with prevalence of physical symptoms [64] and with worse rehabilitation outcome after physical trauma [65].

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Sense Of Coherence scale (SOC)

The sense of coherence (SOC) concept was developed to assess personality- related factors likely to protect people from falling ill. SOC consists of three main components: comprehensibility, manageability and meaningfulness [66]. Poor SOC has an association to major psychosocial risk factors and indicators of perceived mental health problems, use of mental health servic- es and psychiatric diagnosis [67]. In patients with orthopedic injuries [68] a high SOC score predicted a better outcome after surgery after one year.

The Alcohol Use Disorders Identification Test (AUDIT)

Screening for hazardous alcohol use, dependecy symptoms and harmful alcohol use was made by use of Alcohol Use Disorders Identification Test (AUDIT) [69], an instrument with high sensitivity and specificity for detec- tion of current alcohol problems [70].

Sociodemographic variables recorded were gender, age, marital status, years of education and sick-leave at the time of the injury.

y y ( )

SSP scales Description

Somatic trait anxiety Autonomic disturbances, restless, tense Psychic trait anxiety Worrying, anticipating, lacking self-confidence Stress susceptibility Easily fatigued

Lack of assertiveness Lacks ability to be self-assertive in social situations Impulsiveness Acting on the spur of the moment

Adventure seeking Avoiding routine; need for change and action Detachment Avoiding involvement in others; withdrawn Social desirability Socially conforming, friendly, helpful Embitterment Unsatisfied, blaming and envying others Trait irritability Irritable, lacking patience

Mistrust Suspicious, distrusting people´s motives

Verbal trait aggression Getting into arguments, berating people when annoyed Physical trait aggression Getting into fights, starts fights, hits back

Table 5. The scales in Stockholm university Scales of Personality (SSP)

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